Iron is an essential nutrient. Incorporation of iron into prosthetic groups (e.g., heme, sulfur-iron clusters) occurs exclusively in the mitochondrial matrix. Mitochondrial chelatable iron contributes to reactive oxygen species (ROS) formation in several pathophysiological settings, including ischemia/reperfusion and acetaminophen hepatotoxicity. Previous studies show that bafilomycin, ischemia and other stresses cause lysosomes to release Fe2+ and that this iron is subsequently taken up into mitochondria to promote ROS formation.
A need, therefore, exists in the art for fluorescence probes to measures chelatable iron in the mitochondrial matrix useful to researchers studying iron metabolism, for example to assess the mitochondrial chelatable iron pool when mitochondrial membrane potential (ΔΨ) is compromised as during cardiovascular events such as, for example, ischemia.